fig7

Figure 7. Diagram depicts the hypothesized signaling pathways for JNK-paxillin dependent cell migration. Engagement of EGF receptors by EGF triggers rapid activation of JNK, leading to the phosphorylation of paxillin on Ser 178 which might facilitate adhesion turnover thus promoting rapid migration. Upon EGF stimulation, JNK phophorylates also c-Jun which regulates EGFR transcription and β-catenin which delocalizes from the cell-cell contact breaking down the adherens junctions. Paxillin S178A mutant protein might associate with JNK preventing its activation and consequently affecting AP1 activity and EGFR expression. Inactive JNK as well as down-regulation of EGFR result in de-phosphorylation of β-catenin and formation of stabile cell-cell contact in MTLn3 cells